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TRPV1 SUMOylation regulates nociceptive signaling in models of inflammatory pain

Author

Listed:
  • Yan Wang

    (Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine)

  • Yingwei Gao

    (Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine)

  • Quan Tian

    (Wuhan University)

  • Qi Deng

    (Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine)

  • Yangbo Wang

    (Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine)

  • Tian Zhou

    (Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine)

  • Qiang Liu

    (Wuhan University)

  • Kaidi Mei

    (Wuhan University)

  • Yingping Wang

    (Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine)

  • Huiqing Liu

    (Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine)

  • Ruining Ma

    (Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine)

  • Yuqiang Ding

    (Tongji University School of Medicine)

  • Weifang Rong

    (Shanghai Jiao Tong University School of Medicine)

  • Jinke Cheng

    (Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine)

  • Jing Yao

    (Wuhan University)

  • Tian-Le Xu

    (Shanghai Jiao Tong University School of Medicine)

  • Michael X. Zhu

    (The University of Texas Health Science Center at Houston)

  • Yong Li

    (Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine)

Abstract

Although TRPV1 channels represent a key player of noxious heat sensation, the precise mechanisms for thermal hyperalgesia remain unknown. We report here that conditional knockout of deSUMOylation enzyme, SENP1, in mouse dorsal root ganglion (DRG) neurons exacerbated thermal hyperalgesia in both carrageenan- and Complete Freund’s adjuvant-induced inflammation models. TRPV1 is SUMOylated at a C-terminal Lys residue (K822), which specifically enhances the channel sensitivity to stimulation by heat, but not capsaicin, protons or voltage. TRPV1 SUMOylation is decreased by SENP1 but upregulated upon peripheral inflammation. More importantly, the reduced ability of TRPV1 knockout mice to develop inflammatory thermal hyperalgesia was rescued by viral infection of lumbar 3/4 DRG neurons of wild-type TRPV1, but not its SUMOylation-deficient mutant, K822R. These data suggest that TRPV1 SUMOylation is essential for the development of inflammatory thermal hyperalgesia, through a mechanism that involves sensitization of the channel response specifically to thermal stimulation.

Suggested Citation

  • Yan Wang & Yingwei Gao & Quan Tian & Qi Deng & Yangbo Wang & Tian Zhou & Qiang Liu & Kaidi Mei & Yingping Wang & Huiqing Liu & Ruining Ma & Yuqiang Ding & Weifang Rong & Jinke Cheng & Jing Yao & Tian-, 2018. "TRPV1 SUMOylation regulates nociceptive signaling in models of inflammatory pain," Nature Communications, Nature, vol. 9(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03974-7
    DOI: 10.1038/s41467-018-03974-7
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    Cited by:

    1. Yue Xu & Haifeng Zhang & Yuxin Chen & Jordan S. Pober & Min Zhou & Jenny Huanjiao Zhou & Wang Min, 2024. "SRF SUMOylation modulates smooth muscle phenotypic switch and vascular remodeling," Nature Communications, Nature, vol. 15(1), pages 1-18, December.

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